Yan Chen, Li Tao-Sheng
Department of Stem Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Japan.
Department of Stem Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Japan
Anticancer Res. 2018 Feb;38(2):617-621. doi: 10.21873/anticanres.12266.
The effectiveness of chemotherapy is largely limited by drug resistance. In the past few decades, modulation of anticancer drug resistance plays little role in benefit of clinical outcomes due to complex drug resistance mechanisms. Mitophagy, an important mitochondrial quality control system, selectively degrades excessive or damaged mitochondria by autophagy. Accumulating reports are suggesting that dysregulation of mitophagy contributes to neoplastic progression and drug resistance in various types of tumors. Mitophagy was originally thought to be an onco-suppressor that maintains cellular homeostasis and prevents oncogenic transformation. On the other hand, mitophagy promotes cancer cell survival under cytotoxic stress by degrading damaged mitochondria and reducing mitochondrial reactive oxygen species. Therefore, induction and inhibition of mitophagy in cancer drug resistance are controversial. In this review, we summarize current knowledge on the dual role of mitophagy in cancer drug resistance.
化疗的有效性在很大程度上受到耐药性的限制。在过去几十年中，由于耐药机制复杂，对抗癌药物耐药性的调节在改善临床结果方面作用甚微。线粒体自噬是一种重要的线粒体质量控制系统，通过自噬选择性地降解过量或受损的线粒体。越来越多的报道表明，线粒体自噬失调有助于各种类型肿瘤的肿瘤进展和耐药性。线粒体自噬最初被认为是一种肿瘤抑制因子，可维持细胞稳态并防止致癌转化。另一方面，线粒体自噬通过降解受损线粒体和减少线粒体活性氧来促进癌细胞在细胞毒性应激下的存活。因此，在癌症耐药性中诱导和抑制线粒体自噬存在争议。在本综述中，我们总结了目前关于线粒体自噬在癌症耐药性中双重作用的知识。
